Additional studies should help determine if the expression or function of intestinal transmembrane ACE2, other components of the traditional or alternative arm of the renin‐angiotensin system or both, and electrolyte transporters, including ENaC, are impaired in cats with CIE, and whether such effects could explain the association of fibrosis with some of the electrolyte imbalances seen in cats with CIE in our study. This evidence concerns the gene ACE2 and congenital non-bullous ichthyosiform erythroderma.